The purpose of this project is to determine the biochemical aspects of the mechanism(s) by shich gonadotropins stimulate progesterone production by the rat corpus luteum. Immature rats primed with PMSG followed by hCG will be used as a model system for these studies. Ovaries from these rats respond to exogenous LH and jCG in vitro with increased progesterone production. The specific experiments to be performed during the project period include the following: (a)mechanism(s) by which lipoprotein delivered cholesterol is utilized for progesterone synthesis by the corpus luteum tissue and the effect of gonadothropins in this process, (b) investigation of the metabolic fate of hCG receptor after the dissociation of the receptor bound human chorionic gonadotropin (hCG) and the determination of hCG receptor turnover, and (c) to investigate the role of cellular cytoskeletal system especially microfilaments in gonadotropin stimulated progresterone production by the luteal cell. To accomplish objective (a), we will examine the mechanism of induction of lipoprotein receptors in the ovary by hCG and the site of action of hCG in lipoprotein-stimulated progesterone production and the apoprotein specificity of ;ipoprotein binding to the luteal cells. Objective (b) will be accomplished by determining hCG receptor degradation in cultured luteal cells. The turnover of hCG receptor will also be assayed by density shift experiments. Objective (c) will be accomplished by determining the effect of cytochalasin B on cholesterol transport in the luteal cell. We are alos proposing to examine the role of actin phosphorylation in hCG induced stimulation of progesterone synthesis. The outcome from these studies will have important applications in the field of contraception research and the treatment of infertility in females.